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Unit 4 Cardiovascular system
PART 2: THE HEART
ANATOMY OF THE HEART
Location of the Heart
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The heart is located in the mediastinum, the central compartment of the thoracic
cavity (Figure 20.1).
The heart is situated between the lungs in the mediastinum with about two-thirds of
its mass to the left of the midline (Figure 20.1).
The heart is not centered in the mediastinum; about two-thirds of the heart lies to
the left of the midline. The cone-shaped heart has several surfaces:
1. Apex: pointed end of the heart; lies anterior, inferior, and to the left of the
midline.
2. Base: broad portion of the heart; lies posterior, superior, and to the right of
the apex.
3. Anterior surface: deep to the anterior chest wall.
4. Inferior surface: rests on the diaphragm.
5. Right border: faces the right lung.
6. Left border: faces the left lung.
Clinical Connection - because the heart lies between two rigid structures, the
vertebral column and the sternum, external compression on the chest can be used to
force blood out of the heart and into the circulation.
Pericardium
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The heart is enclosed and held in place by the pericardium.
The pericardium consists of an outer fibrous pericardium and an inner serous
pericardium (Figure 20.2a).
The fibrous pericardium is composed of dense irregular connective tissue. It:
1. Anchors the heart to the diaphragm
2. Protects the heart
3. Prevent overfilling of the heart
The serous pericardium is composed of two layers of mesothelium.
The outer parietal layer is fused to the fibrous pericardium.
The inner visceral layer (epicardium) is fused to the surface of the heart.
Between the parietal and visceral layers of the serous pericardium is the pericardial
cavity, a potential space filled with pericardial fluid that reduces friction between the
two membranes.
Clinical Connection -Inflammation of the pericardium is known as pericarditis.
Associated bleeding into the pericardial cavity compresses the heart (cardiac
tamponade) and is potentially lethal.
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Red River College
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Unit 4 Cardiovascular system
Layers of the Heart Wall
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The wall of the heart has three layers: epicardium, myocardium, and endocardium
(Figure 20.2).
The epicardium, or visceral layer of the serous pericardium, is the thin transparent
outermost layer of the heart.
The myocardium is composed of involuntary cardiac muscle fibers that swirl around
the heart in interlacing bundles. The arrangement of the cardiac muscle fibers
produces the strong, smooth, and unified pumping action of the heart.
The endocardium consists of endothelium and connective tissue. It is continuous
with the endothelium lining the large blood vessels attached to the heart and
provides a smooth lining for the heart chambers and the valves.
Chambers of the Heart
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The 4 heart chambers include two superior atria and two inferior ventricles (Figure
20.3).
The atria and ventricles are paired, forming two pumps.
The right atrium and right ventricle pump blood to the lungs.
The left atrium and left ventricle pump blood to the rest of the body.
On the surface of the heart are the auricles and sulci.
The auricles are small pouches on the anterior surface of each atrium that slightly
increase the capacity of each atrium.
The sulci are grooves that contain blood vessels and fat and separate the chambers.
The deep coronary sulcus encircles most of the heart and separates the atria from the
ventricles.
The anterior interventricular sulcus separates the ventricles anteriorly.
The posterior interventricular sulcus separates the ventricles posteriorly.
Right Atrium
 The right atrium forms the right border of the heart (Figures 20.3 - 20.5).
 It receives blood from 3 veins: superior vena cava, inferior vena cava and coronary
sinus.
 Blood passes from the right atrium into the right ventricle through the tricuspid
valve (right atrioventricular valve).
 In the interatrial septum separating the right and left atria is an oval depression, the
fossa ovalis, which is the remnant of the foramen ovale.
 Clinical Connection - Atrial septal defects (ASDs) are due to incomplete closure of
the foramen ovale and, while present in 15 – 25% of adults, are of no clinical
significance. Large clinically significant ASDs allow oxygenated blood from the lungs
to be shunted from the left atrium into the right atrium. Shunting causes
enlargement of the right atrium and ventricle, as well as dilation of the pulmonary
trunk and arteries.
Right ventricle
 The right ventricle forms most of the anterior surface of the heart (Figures 20.3 20.5).
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Unit 4 Cardiovascular system
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Blood passes from the right ventricle to the pulmonary trunk via the pulmonary
semilunar valve.
The right and left ventricles are separated from each other by the interventricular
septum.
Clinical Connection - Ventricular septal defects (VSDs) are the result of incomplete
formation of the interventricular septum. VSDs account for 25% of all forms of
congenital heart disease. Clinically significant VSDs allow oxygenated blood from the
left ventricle to be shunted to the right ventricle, causing enlargement of the right
ventricle, pulmonary trunk, and arteries and cardiac failure.
Left Atrium
 The left atrium forms most of the base of the heart (Figures 20.3 - 20.5).
 It receives oxygenated blood from the pulmonary veins.
 Blood passes from the left atrium to the left ventricle through the through the
bicuspid valve (mitral valve; left atrioventricular valve).
Left ventricle
 The left ventricle forms the apex of the heart (Figures 20.3 - 20.5).
 Blood passes from the left ventricle through the aortic semilunar valve into the aorta.
 During fetal life the ductus arteriosus shunts blood from the pulmonary trunk into
the aorta. At birth it closes and becomes the ligamentum arteriosum.
Myocardial Thickness and Function
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The four chambers’ myocardial thickness varies according to each chamber’s
function (Figure 20.4c).
Atrial walls are thinner than ventricular walls because the atria deliver “low
pressure” blood a short distance to the ventricles.
Ventricular walls are thicker than atrial walls because the ventricles pump blood
under high pressure for great distances.
The walls of the right ventricle are thinner than the left because they pump blood
into the lungs, which are nearby and offer very little resistance to blood flow.
The walls of the left ventricle are thicker because they pump blood through the body
where the resistance to blood flow is greater.
Note in Figure 20.4c that the right ventricle is “C”-shaped, while the left ventricle us
“O”-shaped.
Fibrous Skeleton of the Heart
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The fibrous skeleton of the heart consists of four dense connective tissue rings
located between the atria and ventricles (Figure 20.5).
The functions of the fibrous skeleton are to:
1. Form the foundation for which the heart valves attach
2. Serve as insertion points for cardiac muscle
3. Prevent overstretching of the valves as blood passes through them
4. Act as an electrical insulator that prevents the direct spread of action
potentials from the atria to the ventricles
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Unit 4 Cardiovascular system
HEART VALVES AND CIRCULATION OF BLOOD
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Valves open and close in response to pressure changes as the heart contracts and
relaxes.
Operation of the Atrioventricular (AV) Valves
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Atrioventricular (AV) valves prevent blood flow from the ventricles back into the
atria (Figure 20.6).
AV valves open when atrial pressure exceeds ventricular pressure.
AV valves close when ventricular pressure exceeds atrial pressure.
Back flow is prevented by the contraction of papillary muscles tightening the chordae
tendinae which prevent the valve cusps from everting.
Operation of the Semilunar (SL) Valves
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The semilunar (SL) valves allow ejection of blood from the heart into arteries but
prevent back flow of blood into the ventricles (Figure 20.6).
SL valves open when ventricular pressure exceeds aortic pressure.
SL valves close when aortic pressure exceeds ventricular pressure.
Clinical Connection - A Heart Murmur is an abnormal sound consisting of a flow
noise heard before, between, or after the lubb-dupp or that may mask the normal
sounds entirely. Some murmurs are caused by turbulent blood flow around valves
due to abnormal anatomy or increased volume of flow. Not all murmurs are
abnormal or symptomatic, but most indicate a valve disorder. Certain infectious
diseases, such as rheumatic fever, can damage or destroy heart valves.
Systemic and Pulmonary Circulations
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The left side of the heart is the pump for the systemic circulation. It pumps
oxygenated blood from the lungs out into the vessels of the body.
The right side of the heart is the pump for the pulmonary circulation. It receives
deoxygenated blood from the body and sends it to the lungs for oxygenation.
Figure 20.7 reviews the route of blood flow through the chambers and valves of the
heart and the pulmonary and systemic circulations.
Coronary Circulation
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The flow of blood through the many vessels that pierce the myocardium of the heart
is called the coronary (cardiac) circulation (Figure 20.8a); it delivers oxygenated
blood and nutrients to and removes carbon dioxide and wastes from the
myocardium.
The principal arteries branching from the ascending aorta are the right and left
coronary arteries.
The principle veins terminating in the right atrium as the coronary sinus are the
coronary veins.
Coronary Arteries
 The left coronary artery supplies blood mostly to the left heart (Figure 20.8a).
 Its main branches are:
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Unit 4 Cardiovascular system
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1. Anterior interventricular branch (left anterior descending artery; LAD)
supplies blood to the anterior walls of both ventricles.
2. Circumflex artery supplies blood to the walls of the left ventricle and left
atrium.
The right coronary artery supplies blood mostly to the right heart (Figure 20.8a).
Its main branches are:
1. Atrial branches supply blood to the right atrium.
2. Marginal branch supplies blood to the right ventricle.
3. Posterior interventricular branch (posterior descending coronary artery),
supplies the posterior walls of both ventricles.
The myocardium contains many anastomoses, which provide alternate routes of
blood flow (collateral circuits), which ensures adequate oxygenation of cardiac
muscle.
Coronary Veins
 Superficial to the coronary arteries are the coronary veins (Figure 20.8b). These
veins deliver deoxygenated blood to the right atrium via the coronary sinus. The
main vessels that drain into the coronary sinus are:
1. Great cardiac vein in the anterior ventricular sulcus; drains areas of the heart
supplied by the left coronary artery (left and right ventricles and left atrium)
2. Middle cardiac vein in the posterior interventricular sulcus; drains areas
supplied by the posterior interventricular branch of the right coronary artery
(left and right ventricles)
3. Small cardiac vein in the coronary sulcus; drains right atrium and right
ventricle
 Anterior cardiac veins drain the right ventricle and open directly into the right
atrium.
 Clinical Connection - Coronary artery disease (CAD), or coronary heart disease
(CHD): a condition in which the heart muscle receives an inadequate amount of
blood due to obstruction of its blood supply. It is the leading cause of death in
Canada each year. The principal causes of obstruction include atherosclerosis,
coronary artery spasm, or a clot in a coronary artery. Risk factors for development of
CAD include high blood cholesterol levels, high blood pressure, cigarette smoking,
obesity, diabetes, “type A” personality, and sedentary lifestyle. Partial obstruction of
blood flow in the coronary arteries may cause myocardial ischemia. Ischemia usually
causes hypoxia which may weaken cells without killing them. Angina pectoris is a
severe pain that usually, but not always, accompanies myocardial ischemia. A
complete obstruction to blood flow may result in myocardial infarction (MI),
commonly called a heart attack. Infarction means death of an area of tissue because
of an interrupted blood supply. The resulting damage may be so extensive that the
individual may die.
 Clinical Connection - Atherosclerosis: a process in which smooth muscle cells
proliferate and fatty substances, especially cholesterol and triglycerides (neutral
fats), accumulate in the walls of the medium-sized and large arteries in response to
certain stimuli, such as endothelial damage. Treatment options for CAD include
drugs and coronary artery bypass grafting.
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Unit 4 Cardiovascular system
CARDIAC MUSCLE TISSUE AND THE CARDIAC CONDUCTION SYSTEM
Histology of Cardiac Muscle Tissue
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Compared to skeletal muscle fibers, cardiac muscle fibers are shorter in length,
larger in diameter, branched, and have one nucleus (Figure 20.9).
Cardiac muscles have the same arrangement of actin and myosin, and the same
bands, zones, Z discs, and T tubules as skeletal muscles.
They do have less sarcoplasmic reticulum than skeletal muscles and require Ca+2
from extracellular fluid for contraction.
They do have more mitochondria than skeletal muscles because they depend on
aerobic respiration to make ATP.
Like skeletal muscle cells, cardiac muscle cells cannot divide. This explains why
injured cardiac muscle tissue damaged cannot regenerate.
Cardiac muscles form two separate functional networks in the heart: the atrial and
the ventricular networks.
Fibers within the networks are connected by intercalated discs, which consist of
desmosomes and gap junctions.
Desmosomes lock adjacent cell membranes together.
Gap junctions allow ions to move from one cell to the next, which permits the
spread of action potentials from one cardiac muscle cell to another.
Intercalated discs allow the fibers in the network to work together so that each
network serves as a functional unit.
Autorhythmic Cells: The Conduction System
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Certain cardiac muscle cells are autorhythmic cells because they are selfexcitable. They repeatedly and rhythmically generate spontaneous action potentials
that then trigger heart contractions.
These cells act as a pacemaker to set the rhythm for the entire heart.
They form the conduction system, the route for propagating action potentials
through the heart muscle.
The pathway of cardiac action potentials through the conduction system is as follows
(Figure 20.10):
1. Action potentials arise spontaneously in the sinoartrial (SA) node, which is
located in the right atrium just below the opening of the superior vena cava.
 Each SA node action potential spreads throughout both atria via gap
junctions in the intercalated discs of atrial cardiac muscle cells.
 In other words, each action potential causes both atria to contract in
unison.
2. Action potentials reach the atrioventricular (AV) node (located in the
interatrial septum just in front of the coronary sinus) by traveling through
atrial muscle fibers.
 The velocity of the action potential slows considerably In the AV node
because the pacemaker cells have a smaller diameter there.
 This gives the atria time to completely contract before ventricular
contraction begins.
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Unit 4 Cardiovascular system
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3. The action potential leaves the AV node and enters the atrioventricular
bundle (bundle of His), located in the interventricular septum.
 The AV bundle is the only electrical connection between the atria and
the ventricles.
 The rest of the wall between the atria and ventricles is electrically
insulated by the fibrous skeleton.
4. The action potential travels along the AV bundle and enters the right and left
bundle branches in the interventricular septum, where it travels towards
the apex of the heart.
5. Finally, the action potential is conducted through conduction myofibers
(Purkinje fibers), first to the apex of the heart and then to the rest of the
muscle fibers in both ventricles.
 Then, the ventricular muscle cells contract from apex to base, pushing
blood upward towards the semilunar valves.
 In relation to atrial contraction, the ventricles contract 200 msec
afterwards.
When isolated from other controlling mechanisms, autorhythmic fibers in the SA
node initiate action potentials 90-100 times per minute - faster than any other
autorhythmic cell in the conduction system of the heart.
As a result, action potentials from the SA node stimulate other areas of the
conduction system before they are able to generate an action potential of their own.
In other words, the SA node sets the pace (the fundamental rhythm) of the heart.
Signals from the autonomic nervous system and hormones, such as epinephrine, do
modify the timing and strength of each heartbeat, but they do not establish the
fundamental rhythm.
For example, the parasympathetic nervous system slows SA node pacing to about 75
action potentials per minute. This results in a heart rate of about 75 beats per
minute.
Clinical Connection - Artificial pacemakers stimulate heart muscle and provide a
normal rhythm.
Action Potential and Contraction of Contractile Cells
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Action potentials excite contractile cardiac muscle cells as follows (Figure 20.11):
Depolarization.
 Contractile fibers have a resting membrane potential of –90 mV.
 When an action potential from neighboring cells brings the contractile
cell to threshold, voltage-gated fast Na+ channels open and allow
Na+ to flow into the cell, causing rapid depolarization.
 Within a few milliseconds, fast Na+ channels close and Na+ inflow
decreases.
Plateau.
 After rapid depolarization, some voltage gated K+ channels open
and the cell begins to repolarize.
 But, the cell is prevented from repolarizing by the opening of voltagegated slow Ca2+ channels in the sarcoplasmic reticulum and plasma
membrane, which causes Ca2+ levels to rise in the cytoplasm.
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Unit 4 Cardiovascular system
The influx of Ca2+ into the cytoplasm matches the efflux of K+ from the
cell, causing the cardiac muscle cell to remain depolarized for much
longer than a skeletal muscle cell (about 250 msec compared to about 1
msec).
 As in skeletal muscle fibers, depolarization results in contraction of
cardiac muscle fibers.
 The maintained depolarization during the plateau produces the
contraction force observed in cardiac muscle fibers.
Repolarization.
 After about 250 msec, voltage-gated slow Ca2+ channels close and more
voltage-gated K+ channels open, allowing positive charge (K+) to leave
the cell, and causing it to repolarize.
The refractory period of a cardiac muscle fiber (the time interval when a second
contraction cannot be triggered) is longer than the contraction itself.
Thus, tetanus (maintained contraction) cannot occur in cardiac muscle. Since the
pumping action of the heart depends on alternating contraction and relaxation,
preventing tetanus in cardiac muscle fibers is important. If heart muscle could
undergo tetanus, its pumping action would cease, as would blood flow.
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ATP Production in Cardiac Muscle
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Cardiac muscle relies on aerobic cellular respiration for ATP production (via fatty
acid, glucose, and lactic acid metabolism)..
Cardiac muscle also produces some ATP from creatine phosphate.
Clinical Connection - The presence of creatine kinase (CK) in the blood indicates
injury of cardiac muscle usually caused by a myocardial infarction.
The Electrocardiogram
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Impulse conduction through the heart generates electrical currents that can be
detected at the surface of the body. A recording of the electrical changes that
accompany each cardiac cycle (heartbeat) is called an electrocardiogram (ECG or
EKG).
A normal ECG consists of a P wave, QRS complex, and T wave (Figure 20.12 and
20.13).
1. P wave. A small upward wave on the ECG; represents atrial
depolarization, which spreads from the SA node to both atria. About 100
msec after the P wave begins, the atria contract.
2. QRS complex. Begins as a downward deflection, continues as a large
triangular shaped upward wave, and ends as a downward wave on the ECG. It
represents ventricular depolarization. Shortly after the QRS complex begins,
the ventricles begin to contract.
3. T wave. Dome-shaped upward wave on the ECG; represents ventricular
repolarization. Shortly after the T wave begins, the ventricles relax.
Atrial repolarization cannot usually be visualized on the ECG because it is hidden
within QRS.
P-Q interval - time from the beginning of atrial excitation to the beginning of
ventricular excitation.
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Unit 4 Cardiovascular system
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S-T segment - time when the ventricle is fully depolarized, during the plateau
phase of the impulse.
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Clinical Connection - An ECG is an important tool used to diagnose problems in
heart function because the size of the waves and lengths of the segments can provide
diagnostic clues; for example, an enlarged Q wave or elevated S-T segment may
indicate MI.
Clinical Connection - A dysrhythmia (arrhythmia) is an abnormality or irregularity
in the cardiac rhythm resulting from a disturbance in the conduction system of the
heart, due either to faulty production of electrical impulses or to poor conduction of
impulses as they pass through the system. There are many causes of dysrhythmia,
including congenital defects of the conduction system, degenerative changes,
ischemia and myocardial infarction, fluid and electrolyte imbalances, and the effects
of drug ingestion. Dysrhythmias are not necessarily pathologic; they can occur in
both healthy and diseased hearts. Dysrhythmias exert their harmful effects by
interfering with the heart’s ability to pump blood. Examples of arrhythmias include:
Heart block is a disorder of atrioventricular conduction. Disease and scarring can
damage the conduction pathway between the SA and AV nodes, which can cause the
ventricles to contract out of sync with the atria.
Atrial flutter is a rapid atrial tachycardia with a rate that ranges from 240-450 beats
per minute. Recall that an action potential spreads quickly throughout the atria,
causes atrial contraction, and then dissipates. Atrial flutter is often the result of an
action potential failing to dissipate and depolarizing the atria again.
Fibrillation of the atria or ventricles is the result of chaotic current flow within the
heart muscle and results in an irregular heart rate and rhythm. In ventricular
fibrillation, the ventricle quivers but does not contract, which results in no cardiac
output and no pulse.
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THE CARDIAC CYCLE
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A cardiac cycle is composed of all the events associated with one heartbeat.
Two terms are used when describe events within the cardiac cycle:
Systole, which means “contraction”.
Diastole, which means “relaxation”.
Pressure and Volume Changes during the Cardiac Cycle
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In a normal cardiac cycle, the two atria are in systole while the two ventricles are in
diastole, and vice versa. At 75 beats per minute, each cardiac cycle lasts about 0.8
seconds. The cardiac cycle is divided into three phases:
1. Atrial systole
2. Ventricular Systole
3. Relaxation Period
Refer to Figure 20.14 as you study the phases of the cardiac cycle.
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Unit 4 Cardiovascular system
Atrial Systole
 ECG Connection: from P wave to Q wave (lasts for about 0.1 seconds)
 AV valves: open
 SL valves: closed
 Description: Both atria contract simultaneously, causing the atrial pressure to
increase.
 This forces blood through the AV valves and into the ventricles.
 The ventricles are relaxed and filling with blood (ventricular diastole).
 The SL valves are closed since the pressure in the ventricles is too low to force them
open.
 At rest, atrial contraction contributes about 30% of the total volume of blood that
fills the ventricles.
 Since the end of atrial systole is also the end of ventricular diastole, the total volume
of blood that fills the ventricles at the end of atrial systole is called the enddiastolic volume (EDV; about 130 ml).
 During exercise, the atria contract with more force and more often, thus their
contribution to EDV is greater.
Ventricular Systole
 Ventricular systole lasts about 0.3 seconds and is divided into two periods:
isovolumetric ventricular contraction and ventricular ejection.
 At the same time, the atria are relaxed and filling with blood (atrial diastole).
Isovolumetric Contraction Period
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ECG Connection: begins with R wave(lasts for about about 0.05 seconds)
AV valves: closed
SL valves: closed
Description: Both ventricles begin contracting, causing the ventricular pressure to
increase.
o High ventricular pressure (relative to the atria) closes the AV valves (heard as
“lubb”).
o The SL valves remain closed because the pressure in the ventricles is still too
low to force them open.
Because all heart valves are closed, the volume of the blood in the ventricles remains
constant (isovolumetric).
Ventricular Ejection
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ECG Connection: from S wave to T wave (lasts for about about 0.25 seconds)
AV valves: closed
SL valves: open
Description: Both ventricles continue contracting, and ventricular pressure
continues to increase.
High ventricular pressure forces the SL valves open, and blood is ejected into the
pulmonary trunk and the aorta.
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Unit 4 Cardiovascular system
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Like wringing out a wet rag, the ventricles wring the blood out, beginning at the apex
and moving upward towards the base. This allows for the maximum volume of blood
to be ejected – about 70ml per ventricle.
At the end of ventricular systole about 60 ml of blood remains within each ventricle.
This volume of blood is called the end-systolic volume (ESV).
Stroke volume (SV) is the volume of blood ejected from each ventricle during
systole. It is simple to compute if we know EDV and ESV:
SV= EDV-ESV
At rest, EDV is about 130 ml and ESV is about 60 ml
Thus, SV =130 ml – 60 ml.
Therefore, SV is about 70 ml.
Relaxation Period
 The duration of the relaxation period is variable; at rest, it lasts about 0.4 seconds. It
is divided into two periods: isovolumetric ventricular relaxation and passive
ventricular filling.
 During the relaxation period, both atria and ventricles are in diastole and are filling
with blood.
Isovolumetric Ventricular Relaxation
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ECG Connection: begins at end of T wave
AV valves: closed
SL valves: closed
Description: Both ventricles begin to relax , and ventricular pressure begins to
decrease to increase.
Low ventricular pressure (relative to the pulmonary trunk and aorta) closes the SL
valves (heard as “dupp”).
The AV valves remain closed because the pressure in the ventricles is still too high to
allow them to open.
Because all heart valves are closed, no blood flows into the ventricles.
Passive Ventricular Filling
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ECG Connection: after T wave to next P wave
AV valves: open
SL valves: closed
Description: Both ventricles continue to relax , and ventricular pressure continues to
decrease.
As blood flows into the atria, atrial pressure increases until it exceeds ventricular
pressure.
This forces the AV valves open, and blood fills the ventricles.
Passive ventricular filling is the main way the ventricles are filled, accounting for
about 70% of filling. The remaining 30% comes from the next cardiac cycle, which
beginning, again, with atrial systole.
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Unit 4 Cardiovascular system
Some Final Points about the Cardiac Cycle
 As the body’s metabolic demands increase, the demands on the heart to deliver
blood to body tissues increases as well.
 The heart meets these demands by increasing its rate and force of contraction.
 During the cardiac cycle (one heart beat), the durations of atrial and ventricular
systole remain relatively unchanged regardless of changes in heart rate.
 Therefore, as heart rate increases, the length of each individual cardiac cycle
decreases because the length of each relaxation period decreases.
CARDIAC OUTPUT
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Body cells need specific amounts of oxygen each minute to maintain health and life.
As they work harder they require greater amounts of oxygen, and thus more blood.
Since the body’s need for oxygen varies with the level of activity, the heart’s ability to
discharge oxygen-carrying blood must also be variable.
 Cardiac output (CO) is the volume of blood ejected from the ventricle into the
aorta or pulmonary trunk each minute. Cardiac output equals the stroke volume,
multiplied by the heart rate (# of beats/minute).
CO = SV X HR
At rest CO = 70 ml/beat X 75 beats/minute
At rest CO = 5.25 L / minute
 At rest, the volume of blood pumped by the heart each minute is approximately
equal to total blood volume.
 During exercise, the volume of blood that the tissues require increases. Thus CO
must increase.
 The body can change cardiac output by regulating either stroke volume or heart rate.
 Cardiac reserve is the ratio between the maximum cardiac output a person can
achieve and the cardiac output at rest. A cardiac reserve of 4 –5 times resting CO is
average.
 This translates into a CO of 21 – 26 L of blood pumped by each ventricle per minute
during maximal activity.
 Elite endurance athletes have a cardiac reserve of 7-8 times resting CO. This
translates into a CO of 36 – 42 L of blood pumped by each ventricle per minute
during maximal activity.
 People with severe heart disease may have little or no cardiac reserve. This limits
their ability to carry out even the simplest activities associated with daily living.
Regulation of Stroke Volume
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Three factors regulate stroke volume:
1. Preload, the degree of stretch on the heart before it contracts.
2. Contractility, the forcefulness of contraction of individual ventricular
muscle fibers.
3. Afterload, the pressure that must be exceeded before ventricular ejection
can occur.
Preload: Effect of Stretching
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Red River College
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Unit 4 Cardiovascular system
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A greater preload (stretch) on cardiac muscle prior to contraction increases its force
of contraction.
Preload can be compared to the stretching of a rubber band; the more the rubber
band is stretched, the more forcefully it will snap back.
Within limits, the more the heart fills with blood during diastole, the greater the
force of contraction during systole. This relationship is called the Frank-Starling
Law of the Heart.
Preload is proportional to EDV; normally, the greater the EDV, the more forceful the
next contraction.
Two factors determine preload:
1. Duration of ventricular diastole
As heart rate increases, the duration of diastole decreases
As the duration of diastole decreases, filling time decreases
As filling time decreases, EDV decreases
As EDV decreases, preload decreases
As preload decreases, the force of contraction decreases
2. Venous return
As venous return increases, blood flow into the ventricles increases
As more blood flows into the ventricles, EDV increases
As EDV increases, preload increases
As preload increases, the force of contraction increases
This relationship between EDV and preload equalizes the output of the right and left
ventricles and keeps the same volume of blood flowing to both the systemic and
pulmonary circulations.
If the left side of the heart pumps a little more blood than the right side, the volume
of blood returning to the right ventricle (venous return) increases. The increased
EDV causes the right ventricle to contract more forcefully on the next beat, bringing
the two sides back into balance.
Contractility
 Myocardial contractility is the strength of contraction at any given preload.
 Any chemical that affects contractility is called an inotropic agent.
 Positive inotropic agents (e.g. epinephrine) increase contractility and SV.
 Often work by promoting Ca2+ inflow
 Negative inotropic agents (e.g. acetylcholine) decrease contractility and SV.
 Often work by inhibiting Ca2+ inflow (e.g. calcium channel blockers).
 The ANS and endocrine system affect myocardial contractility.
 The sympathetic nervous system and adrenal medulla of the endocrine system
release epinephrine, which increases myocardial contractility.
 The parasympathetic system releases ACh, which decreases myocardial contractility.
Afterload
 Afterload is the pressure that the ventricles must overcome to open the SL valves.
 Anything that impedes blood flow can increase afterload (e.g. hypertension).
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J. Taylor
Red River College
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Unit 4 Cardiovascular system
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If afterload increases, the ventricles spend more time in isovolumetric contraction
and less time in ventricular ejection.
Thus increased afterload decreases stroke volume and causes more blood to remain
in the ventricles at the end of systole (increased ESV).
Congestive Heart Failure – When Stroke Volume Regulation Breaks Down
 In congestive heart failure (CHF), there is a loss of pumping efficiency by the heart.
 Causes of CHF include coronary artery disease, hypertension, myocardial infarction,
and valvular defects.
 Let’s look at one cause, hypertension:
 Long-term hypertension increases the afterload, resulting in an increased ESV.
 Increased ESV gradually leads to increased EDV.
 Increased EDV increases preload.
 Initially, preload promotes increased force of contraction (Frank Starling’s Law)
 As preload increases further, the heart is overstretched and contracts less forcefully
(decreased myocardial contractility)
 CHF is the result of a positive feedback loop: less effective pumping leads to even
lower pumping capability.
 Often, one side of the heart starts to fail before the other.
 Right heart failure represents failure of the right heart to pump blood into the
pulmonary circulation, and ultimately the lungs. Consequently, blood backs up in the
systemic circulation, causing peripheral edema.
 Left heart failure represents failure of the left heart to pump blood into the systemic
circulation. Consequently, blood backs up in the pulmonary circulation, causing
pulmonary edema.
Regulation of Heart Rate
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Regulating heart rate is the body’s principal mechanism of short-term control over
cardiac output.
Several factors contribute to regulation of heart rate (Figure 20.16).
1. The autonomic nervous system: sympathetic and parasympathetic divisions
2. Chemicals: hormones and ions
3. Other factors such as age, gender, physical fitness, and body temperature.
Autonomic Regulation of Heart Rate
 Nervous control of the cardiovascular system stems from the cardiovascular
center in the medulla oblongata (Figure 20.16).
 Proprioceptors, baroreceptors, and chemoreceptors monitor factors that influence
the heart rate.
 Sympathetic impulses increase heart rate and force of contraction.
 Parasympathetic impulses decrease heart rate but have little effect on contractility.
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J. Taylor
Red River College
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Unit 4 Cardiovascular system
Chemical Regulation of Heart Rate
 The adrenal medulla releases two hormones that affect heart rate: epinephrine and
norepinephrine.
 Epinephrine and norepinephrine increase heart rate and contractility.
 Thyroid hormone also increases heart rate and myocardial contractility. One clinical
sign of hyperthyroidism is an elevated resting heart rate (tachycardia).
 Ion concentrations (especially Na+, K+, Ca+2) also affect heart rate.
 Elevated blood levels of Na+ and K+ decrease heart rate and contractility.
 Elevated blood levels of Ca2+ increase heart rate and contractility.
Other Factors in Heart Rate Regulation
 Other factors such as age, gender, physical fitness, and temperature affect heart rate:
 The very young have an elevated resting heart rate that declines with age. Senior
citizen often develop an elevated heart rate.
 Adult females tend to have a slightly higher resting heart rate than adult males.
 Regular exercise tends to decrease the resting heart rates of both sexes. A physically
fit person may exhibit a heart rate below 60 beats per minute (bradycardia).
 Increased body temperature (e.g. during a high fever or during strenuous exercise;
hyperthermia) can raise heart rate. Decreased body temperature (hypothermia) can
lower heart rate.
For a review of all of the factors that increase cardiac output, see Figure 20.17
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J. Taylor
Red River College
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